- Lung cancer can be deadly, but experts are continuing to develop diverse and more targeted treatment options.
- One area of interest is how to treat lung cancers that are caused by the mutations of a specific gene.
- Data from a new study found that the mutated KRAS gene influences the lipids and metabolism of lipids in lung cancer. Their findings suggest that targeting components of lipid metabolism and synthesis could be part of effective lung cancer treatments.
Lung cancer can be both deadly and difficult to treat.
Experts’ understanding of lung cancer has significantly expanded in recent years with developing new treatment options being a priority.
As options for specific, targeted treatments emerge, experts are hopeful that the prognosis for people with lung cancer will continue to improve.
In a recent
There are a few different
The type of lung cancer someone has helps doctors determine treatment options and predict prognosis.
One of the most common types of lung cancer is non-small cell lung cancer (NSCLC).
Dr. Misty D. Shields, an oncology expert at Indiana University Health, explained to Medical News Today:
“Lung cancer is the leading cause of cancer-related deaths, and there are more than 2 million patients diagnosed with lung cancer each year worldwide. Most patients diagnosed with lung cancer have a history of smoking, but ~20% of patients have never smoked in their lifetime.”
Some people with lung cancer have a distinct gene mutation that occurs.
Specifically, mutations in the KRAS gene can happen in people with lung cancer. As the American Lung Association notes, “About 20-25% of lung cancer patients have some kind of KRAS mutation.”
Researchers are still working to understand how KRAS gene mutations impact lung cancer and how to develop
One area of interest is how the KRAS gene mutation affects fatty acid metabolism.
Researchers in the recent study examined a few different components of lung cancer with the KRAS mutation.
First, they said they found that lung cancer with the mutant KRAS gene had a unique lipid profile.
They further reported that lung cancer with the KRAS gene mutation was dependent on a specific enzyme, FASN, that is involved in fatty acid synthesis. Researchers then worked to target this enzyme and its function.
They reported that blocking FASN promoted the death of specific lung cancer cells. For example, FASN inhibitors contributed to ferroptosis, a specific type of cell death.
Ultimately, researchers hope that this data will promote the development of specific targeted lung cancer treatments.
While a bit technical, Shields provided the following summary of the study’s research to MNT:
“The authors demonstrate KRAS mutant NSCLC requires a rate-limiting enzyme, FASN, for lipid metabolism, through the Lands cycle, to cope with oxidative stress and deflect ferroptosis for cancer cell survival. This novel research highlights that targeting fatty acid synthesis with FASN inhibitors may be a promising approach for KRAS mutant NSCLC.”
The study provided data to set up future research and clinical trials.
Limitations to the study were based on the methods researchers utilized. For example, their work mainly included mouse models, so further research will be needed to confirm the findings.
The data can also examine lifestyle and health factors influencing KRAS gene lung cancer.
Clinical trials can test the effectiveness of treatment for people with lung cancer with the KRAS gene mutation.
Dr. Pier Paolo Scaglioni, a study author and professor of medicine at the University of Cincinnati College of Medicine, said he was excited about the potential treatment experts could develop from this research:
“There is a great interest in developing drugs that target the metabolisms of cancer cells. Thus, yes, there are therapeutic implications. We have carried out a phase I trial with a FASN inhibitor and are performing a phase II trial in lung cancer patients with the KRAS mutation.”
Shields noted that further research could also examine the effectiveness of treatments involving FASN inhibitors and how well they will work alone or with other treatments.
“Future clinical investigations with FASN inhibitors are needed to understand the efficacy, tolerability, and biology of these novel agents alone and in combination for lung cancer,” she explained.
Scaglioni noted the following components of future research to MNT:
“This is just the beginning: we should figure out if there are mechanisms that mediate resistance to treatment. Also, it will be important to know if there are combination treatments that synergize with FASN inhibition. A related area of investigation is to determine whether stimulation of ferroptosis is a therapeutic strategy.”
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